Studies in Carbohydrate Metabolism Following Guanidine Deglycogenation
Fritz Bischoff and
M. Louisa Long
(From The Chemical Laboratory of the Potter Metabolic Clinic, Santa Barbara Cottage Hospital, Santa Barbara)
1. By means of the diguanidino-polymethylenes it is possibleto deplete the glycogen reserves of the liver and destroy thepower of this organ to store glycogen, without destroying thepower of the muscles to utilize glucose either by its disappearanceor storage as glycogen. It is also possible to deplete the glycogenreserves and prevent the storing of glycogen at a hyperglycemiclevel for both liver and muscle, without destroying the powerto utilize glucose.
2. Insulin increases the utilizationof glucose at normalor hyperglycemic levels in guanidine deglycogenatedrabbitswith or without storing glycogen.
3. Adrenalinis able to decrease the utilization of injectedglucose in animalsin which the liver has been depleted of glycogenand has lostthe power of storing glycogen through guanidinederivatives,showing that normal adrenalin hyperglycemia isnot entirelydue to an increased output of glucose by the liver.
4. Adrenalinincreases the blood lactic acid and insulinis without effectupon the blood lactic acid of rabbits sufferingguanidine deglycogenation.
5. Adrenalin increases the blood lactic acid in rabbitswhose liver and muscle glycogen reserves have been depleted(less than .01 per cent) by guanidine derivatives.